Many people do not consider obesity a disease—in fact, I am a skeptic myself. It seems so clear to me how obesity can be resolved if people simply modified their eating behaviors. For example, when are you eating, how much are you eating, what kinds of foods are you eating, these are all questions that could allow eating behaviors to change to be more healthy based on what nutritionists and dietician have discovered.
However, when I compare obesity to addiction, I understand how it can be seen as a disease. Addiction might start with inappropriate drug-using behaviors. However, it escalates when it becomes abused, and that substance abuse or chemical dependency illustrates malfunctioning neural transmission. Food can also be a substance that becomes abused when processes in the brain no longer work like they should.
A related disease to obesity is Binge Eating Disorder (BED). BED is a medical condition characterized by ingestion of large amounts of food due to loss of control while eating. According to Ginger Nicol, MD, weight gain and obesity can result in 40% of individuals with BED, because it does not involve compensatory behaviors.
Why do only 40% of all who meet criteria for BED weight gain and obesity? Perhaps it is due to an individuals neurochemistry and how it is different from another’s. For example, an non-obese individual with BED may experience more weight gain than another non-obese individual with BED, because that person has a genetic predisposition for weight gain to due their parents’ obesity.
It is also worth noting the metabolic mechanisms BED:
- Exacerbate hunger
- Prevent satiety
- Drive food preferences
So how do these mechanisms become malfunctioning in people with obesity and BED?
A 2013 journal article by Vogt and Bruning in Trends in Endocrinology and Metabolism explain how abnormal insulin and leptin signaling lead to obesity. Insulin and leptin are both released in the PNS and CNS to regulate food intake. Both substances work to maintain energy homeostasis by signaling fullness to the hypothalamus when food intake can cease.
Leptin and insulin levels actually rise with increased for intake, and this rising levels contribute to resistance. Leptin and insulin resistance leads to lack of satiety excessive food intake.
The endocannabinoid system also plays a role in obesity and BED. According to a 2015 study by Fattore, the endocannabinoid system is critical in changing energy balance by modulating food intake. In fact, it is commonly known that administration of cannabis increases appetite. Various human and animal studies have shown that CB1R agonists increase total food intake, particularly consumption of palatable foods. As a result, the a current treatment drug for obesity and BED is rimonabant, a endocannabinoid receptor blocker.
In addition, there is a connection between the endocannabinoid system and the endocrine system. Leptin inhibits endocannabinoid production by the hypothalamus. In the case of leptin resistance, endocannabinoids would be overproduced and food intake will increase.
All in all, there is much still to be discovered on the topic of obesity, and studying BED in conjunction may provide additional insights to the investigation.
